Leukotrienes, the 5'-lipoxygenase metabolites of arachidonic acid, are pulmonary vasoconstrictors. The inhibition of leukotriene action by FPL 57231, a leukotriene end organ antagonist, markedly increases pulmonary blood flow in the normal fetus and prevents hypoxic pulmonary vasoconstriction in newborn and adult animals. Leukotrienes have been isolated in the lung lavage fluid taken from perfused rat lungs during hypoxic pulmonary vasoconstriction and from infants with persistent pulmonary hypertension syndrome. These studies suggest that leukotrienes may have an important role in maintaining the increased pulmonary vascular resistance in the fetus. At birth, with the initiation of ventilation there is a decrease in pulmonary vascular resistance and an increase in pulmonary blood flow. Prostaglandins, the cyclo-oxygenase metabolites of arachidonic acid, probably at least in part mediate this ventilation induced fall in pulmonary vascular resistance. Prostacyclin, a pulmonary vasodilator, is released from the lung with the initiation of ventilation. PGD2 specifically lowers pulmonary arterial pressure in pump perfused fetal goat lungs and in newborn lambs with hypoxic pulmonary hypertension. It produces mild pulmonary vasoconstriction in older animals. This study has several purposes: 1) to define the interaction between leukotrienes and prostaglandins in the control of the perintal pulmonary circulation; 2) to further define the role of leukotriene pulmonary hypertension induced by hypoxia and thromboxane activity 3) to determine whether the production of leukotrienes and prostaglandins by the lung is altered by different oxygen environments. A better understanding of the interaction between the prostaglandins and the leukotrienes is important in understanding the mechanisms that control pulmonary vascular resistance in the perinatal period and in the treatment of infants with persistent pulmonary hypertension syndrome.